By SANDY SMOLAN I’ve long been interested in the capacity of storytelling and journalism to transport an audience. Shooting my first documentary in North Africa 35 years ago, I used multiple projectors and screens to create an immersive experience. The approach at the time was experimental and while I moved on to more traditional storytelling in features, television and documentaries, I always held on to the idea of using immersive environments to transport viewers and allow them to experience an expanded vision of the world. They surrounded the divers and started clicking — they seemed to be saying hello. Then last year I visited the virtual reality lab at Stanford, which is at the fore of contemporary immersive journalism. I realized that V.R. had the potential to become a powerful new form of storytelling, and the medium has been evolving faster than anyone had ever expected. After I read James Nestor’s book “Deep,” about free diving and the human connection to the ocean, I realized that the combination of stunning imagery and the way in which a team of researchers were studying the language of whales and dolphins by free diving with them would translate perfectly to V.R. I had never forgotten my first open water dive in the Caribbean with my father when I was 17 and the transcendent experience of being suspended 30 feet beneath the surface, midway between the boat above us and the white sand of the ocean floor below. Now my son has become a free diver and as I recently watched him dive silently, on a single breath, his body elongated with outsize fins, unencumbered by tanks, regulators and the noise of escaping bubbles, I saw what James so eloquently described in his book — a human being interacting with the ocean and marine life in a manner few people can ever experience. © 2017 The New York Times Company

Keyword: Animal Communication; Hearing
Link ID: 24032 - Posted: 09.04.2017

Robin McKie Science Editor People who use genetic tests to trace their ancestry only to discover that they are at risk of succumbing to an incurable illness are being left to suffer serious psychological problems. Dementia researchers say the problem is particularly acute for those found to be at risk of Alzheimer’s disease, which has no cure or effective treatment. Yet these people are stumbling upon their status inadvertently after trying to find their Viking, Asian or ancient Greek roots. “These tests have the potential to cause great distress,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. “Companies should make counselling available, before and after people take tests.” The issue is raised in a paper by Middleton and others in the journal Future Medicine. A similar warning was sounded by Louise Walker, research officer at the Alzheimer’s Society. “Everyone has a right to know about their risk if they want to, but these companies have a moral responsibility to make sure people understand the meaning and consequences of this information. Anyone considering getting genetic test results should do so with their eyes open.” Alzheimer’s is linked to the build-up in the brain of clumps of a protein called amyloid. This triggers severe memory loss, confusion and disorientation. One gene, known as ApoE, affects this process and exists in three variants: E2, E3 and E4. Those possessing the last of these face an increased chance of getting the disease in late life. © 2017 Guardian News and Media Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 24031 - Posted: 09.04.2017

Marsha Lederman Santiago Ramon y Cajal wanted to be an artist, but his father, a physician and anatomy teacher, wanted his son to follow in his medical footsteps. It's a familiar story of family dynamics, but what wound up happening in this case was revolutionary. Cajal, who was born in 1852 in northeastern Spain, did ultimately go into medicine, as his father wished. He became a pathologist, histologist and neuroscientist. But he also applied his artistic skills to his area of interest. His hand-drawn illustrations of the brain, based on what he saw through the microscope using stained brain tissue (thanks to a technique developed by his contemporary, the Italian histologist Camillo Golgi) were pioneering. Cajal, who won the Nobel Prize in 1906 (along with Golgi), is known as the father of modern neuroscience. More than a century after he made them, his drawings are still used to illustrate principles of neuroscience. "When I was a student … everybody would start their talk, 'as first shown by Cajal,'" says Brian MacVicar, co-director at Djavad Mowafaghian Centre for Brain Health and Canada Research Chair in Neuroscience at the University of British Columbia. When MacVicar learned that an exhibition of Cajal's drawings was being planned by neuroscience colleagues in Minnesota along with the Weisman Art Museum at the University of Minnesota, he was immediately on a mission: to bring the drawings to Vancouver. He finally extracted a yes from the show organizers, but not operating in the art world, MacVicar wasn't sure who might want to exhibit them in Vancouver. The answer turned out to be right in his backyard – or at least, a few blocks away on campus. Scott Watson, director/curator of the Morris and Helen Belkin Art Gallery at the University of British Columbia, had seen Cajal's work at the Istanbul Biennial in 2015 – and understood their appeal and value.

Keyword: Brain imaging
Link ID: 24030 - Posted: 09.04.2017

Sara Reardon Scientists studying human behaviour and cognitive brain function are up in arms over a plan by the US National Institutes of Health (NIH) to classify most studies involving human participants as clinical trials. An open letter sent on 31 August to NIH director Francis Collins says that the policy could “unnecessarily increase the administrative burden on investigators,” slowing the pace of discovery in basic research. It asked the NIH to delay implementation of the policy until it consulted with the behavioural science community. As this article went to press, the letter had garnered 2,070 signatures. “Every scientist I have talked to who is doing basic research on the human mind and brain has been shocked by this policy, which makes no sense,” says Nancy Kanwisher, a cognitive neuroscientist at the Massachusetts Institute of Technology in Cambridge, who co-wrote the letter with four other researchers. The policy is part of an NIH clinical trial reform effort started in 2014 to ensure that all clinical results were publicly reported. The policy is scheduled to go into effect in January 2018. Its definition of a clinical trial included anything involving behavioural ‘interventions’, such as having participants perform a memory task or monitor their food intake. Such studies would need special evaluation by NIH review committees and institutional ethics review boards; and the experiments would need to be registered online in the clinicaltrials.gov database. © 2017 Macmillan Publishers Limited

Keyword: Miscellaneous
Link ID: 24029 - Posted: 09.02.2017

By Meghana Keshavan, Inflammation has become one of the hottest buzzwords in medical science, pointed to as a culprit in causing or aggravating conditions ranging from allergy to autism to Alzheimer’s disease. But it’s far from clear that standard anti-inflammatory drugs, which have been around for decades, will help patients with those conditions, especially since they often come with dangerous side effects. So in labs across the country, scientists are trying to puzzle through the basic biology, understanding how inflammation leads to disease — and whether it’s possible to develop drugs that could interrupt that process. The latest evidence of inflammation’s broad role in disease came this past week, when a global clinical trial of 10,000 patients who had previous heart attacks showed that an anti-inflammatory drug from Novartis reduced their risk of further heart attacks or strokes. A surprise side effect: The drug also sharply cut the risk of lung cancer. That finding still needs to be confirmed with more research. But lead investigator Dr. Paul Ridker, a cardiologist at Brigham and Women’s Hospital, said he saw the trial as a clear indication of inflammation’s role in spurring cancer growth. The results, he said, turn “the way people look at oncology upside down.” Although inflammation has been studied for decades, there’s still a lot left to learn about this complex physiological condition. It’s basically an unnecessary state of hyperactivity in the body, in which the immune system’s reserve capacity is thrown into overdrive. This excess immune activation sends the wrong cellular signals to various parts of the body — and can wind up worsening conditions like diabetes, Alzheimer’s, and potentially even cancer. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 24028 - Posted: 09.02.2017

By JOSH KATZ The first governmental account of nationwide drug deaths in 2016 shows overdose deaths growing even faster than previously thought. Drug overdoses killed roughly 64,000 people in the United States last year, according to the first governmental account of nationwide drug deaths to cover all of 2016. It’s a staggering rise of more than 22 percent over the 52,404 drug deaths recorded the previous year — and even higher than The New York Times’s estimate in June, which was based on earlier preliminary data. Drug overdoses are expected to remain the leading cause of death for Americans under 50, as synthetic opioids — primarily fentanyl and its analogues — continue to push the death count higher. Drug deaths involving fentanyl more than doubled from 2015 to 2016, accompanied by an upturn in deaths involving cocaine and methamphetamines. Together they add up to an epidemic of drug overdoses that is killing people at a faster rate than the H.I.V. epidemic at its peak. This is the first national data to break down the growth by drug and by state. We’ve known for a while that fentanyls were behind the growing count of drug deaths in some states and counties. But now we can see the extent to which this is true nationally, as deaths involving synthetic opioids, mostly fentanyls, have risen to more than 20,000 from 3,000 in just three years. Deaths involving prescription opioids continue to rise, but many of those deaths also involved heroin, fentanyl or a fentanyl analogue. There is a downward trend in deaths from prescription opioids alone. At the same time, there has been a resurgence in cocaine and methamphetamine deaths. Many of these also involve opioids, but a significant portion of drug deaths — roughly one-third in 2015 — do not. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24027 - Posted: 09.02.2017

By Matt Reynolds Putting on a brave face won’t fool this algorithm. A new system that rates how much pain someone is in just by looking at their face could help doctors decide how to treat patients. By examining tiny facial expressions and calibrating the system to each person, it provides a level of objectivity in an area where that’s normally hard to come by. “These metrics might be useful in determining real pain from faked pain,” says Jeffrey Cohn at the University of Pittsburgh in the US. The system could make the difference between prescribing potentially addictive painkillers and catching out a faker. Objectively measuring pain levels is a tricky task, says Dianbo Liu, who created the system with his colleagues at the Massachusetts Institute of Technology. People experience and express pain differently, so a doctor’s estimate of a patient’s pain can often differ from a self-reported pain score. In an attempt to introduce some objectivity, Liu and his team trained an algorithm on videos of people wincing and grimacing in pain. Each video consisted of a person with shoulder pain, who had been asked to perform a different movement and then rate their pain levels. The result was an algorithm that can use subtle differences in facial expressions to inform a guess about how a given person is feeling. Certain parts of the face are particularly revealing, says Liu. Large amounts of movement around the nose and mouth tended to suggest higher self-reported pain scores. © Copyright New Scientist Ltd.

Keyword: Pain & Touch; Emotions
Link ID: 24026 - Posted: 09.02.2017

By Brian Levine, Carrie Esopenko There are two ways to go about studying a disease. Let’s call them the retrospective and prospective methods. In the retrospective method, scientists identify individuals with the disease and ask about the circumstances that led to the illness. In the prospective method, they start with a representative sample of people and track them over time to see who develops the disease. Both methods have yielded important discoveries, but the retrospective method is much more prone to distortion than the prospective method. Consider the following example. Using the retrospective method, 100 percent of alcoholics drink alcohol. Yet drinking alcohol does not necessarily lead to alcoholism, as can be determined by the prospective method in which it can be seen that the proportion of those who enjoy alcoholic drinks and become alcoholics is less than 100 percent. Boston University’s Chronic Traumatic Encephalopathy (CTE) Center recently reported that 99 percent of NFL alumni who made brain donations at the time of death have CTE (a similar finding was reported in 2013). While researchers acknowledge that those who make brain donations are not representative of retired NFL players (much less those with sports-related concussions in general) it is remarkably easy to make the same mistake as in the alcoholism example—that is, making the assumption that this finding generalizes to the broader population of athletes exposed to concussion. © 2017 Scientific America

Keyword: Brain Injury/Concussion
Link ID: 24025 - Posted: 09.02.2017

By Aggie Mika A drawing based on one of Ramón y Cajal’s “selfies,” with his pyramidal neuron illustrations around him. According to Hunter, Ramón y Cajal obsessively took photos of himself throughout his life. DAWN HUNTER, WITH PERMISSIONIt was in the spring of 2015 when Dawn Hunter saw Santiago Ramón y Cajal’s century-old elaborate drawings of the nervous system in person for the first time, at the late scientist’s exhibit within the National Institutes of Health. She was instantly compelled to recreate his ornate illustrations herself. “I just immediately started drawing [them] because they were so beautiful,” says Hunter, a visual art and design professor at the University of South Carolina. “His drawings in person were even more amazing than I thought they were going to be.” Ramón y Cajal’s drawings first caught Hunter’s eye while doing research for a neuroanatomy textbook she was asked to illustrate in 2012. Ramón y Cajal, hailed by many as the father of modern neuroscience, depicted the inner workings of the brain through thousands of intricate illustrations before his death in 1934. He first posited that unique, inter-connected entities called neurons were the central nervous system’s fundamental unit of function. A recreation of Ramón y Cajal Cajal’s retina depiction. “His retina drawing is particularly interesting because he combines both of his main drawing techniques. . . . Part of the drawing is designed and drawn out preliminarily and part of it is drawn from observation,” says Hunter.DAWN HUNTER, WITH PERMISSIONWhile recreating his work, Hunter was able to shed unprecedented light on how he went about his craft. “Some neuroscientists erroneously think that he traced all of his drawings from a projection, which he did not,” she says. This involves expanding a magnified image of the specimen being viewed under the microscope onto the table using a drawing tube or camera lucida. While he did use this tool in certain instances, she says, he drew some of his drawings, like his famous pyramidal neurons, “through his observation with his eye,” a technique known as perceptual drawing. © 1986-2017 The Scientist

Keyword: Brain imaging
Link ID: 24024 - Posted: 09.02.2017

By Mitch Leslie When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effect—protecting against Parkinson’s disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didn’t take the drug, a study reveals. “I’m sure it’s going to be a landmark paper,” says neurologist Joseph Jankovic of Baylor College of Medicine in Houston, Texas, who wasn’t involved in the research. In Parkinson’s disease, gobs of the protein α-synuclein accumulate in certain brain cells and may kill them. Scientists have tried to craft drugs that speed the elimination of the protein or prevent it from clumping. Neurologist and genomicist Clemens Scherzer of Harvard Medical School in Boston and colleagues decided to try a different strategy. “We wanted to find a drug that could turn down the production of α-synuclein,” he says. To identify promising compounds, the team grew human nerve cells in the lab and tested whether more than 1100 medications, vitamins, dietary supplements, and other molecules altered their output of α-synuclein. Three of the drugs that cut the protein’s production, including salbutamol, work by stimulating the b2-adrenoreceptor—a molecule on some body cells that triggers a variety of effects, including relaxing the airways. The researchers found that these drugs appear to alter how tightly the DNA containing the α-synuclein gene coils, and thus whether the gene is active. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 24023 - Posted: 09.01.2017

You may well be yawning just reading this - it's contagious. Now researchers have looked at what happens in our brains to trigger that response. A University of Nottingham team found it occurs in a part of the brain responsible for motor function. The primary motor cortex also plays a part in conditions such as Tourette's syndrome. So the scientists say understanding contagious yawning could also help understand those disorders too. Contagious yawning is a common form of echophenomena - the automatic imitation of someone else's words or actions. Echophenomena is also seen in Tourette's, as well as in other conditions, including epilepsy and autism. To test what's happening in the brain during the phenomenon, scientists monitored 36 volunteers while they watched others yawning. In the study, published in the journal Current Biology, some were told it was fine to yawn while others were told to stifle the urge. The urge to yawn was down to how each person's primary motor cortex worked - its "excitability". And, using external transcranial magnetic stimulation (TMS), it was also possible to increase "excitability" in the motor cortex and therefore people's propensity for contagious yawns. Georgina Jackson, professor of cognitive neuropsychology who worked on the study, said the finding could have wider uses: "In Tourette's, if we could reduce the excitability we might reduce the ticks, and that's what we are working on." Prof Stephen Jackson, who also worked on the research, added: "If we can understand how alterations in cortical excitability give rise to neural disorders we can potentially reverse them. "We are looking for potential non-drug, personalised treatments, using TMS that might be effective in modulating imbalances in the brain networks." © 2017 BBC

Keyword: Attention
Link ID: 24022 - Posted: 09.01.2017

By Clare Wilson Some people who are blind can echolocate like bats, making clicks with their mouths that help them understand the environment around them. Now researchers are beginning to understand how this works, so non-sighted people may one day be able to learn the technique. While many people who are blind get information from ambient echoes, only a few make noises themselves to echolocate. Some, such as Daniel Kish (pictured), are so proficient they can draw a sketch of a room after clicking their way around it, or even go mountain biking along unfamiliar routes. Daniel Kish: Blind children should be allowed to echolocate like me Previous research revealed that this human echolocation involves some brain areas that are used for vision in sighted people. Kish, who was blind almost from birth, thinks he experiences the sensations as something akin to images. “It’s not computational. There’s a real palpable experience of the image as a spatial representation – here are walls, here are the corners, here is the presence of objects.” In the latest study, Lore Thaler of Durham University, UK, and her team carried out the first in-depth acoustic analysis of the mouth clicks. They worked with Kish and two other blind echolocators from the Netherlands and Austria. © Copyright New Scientist Ltd.

Keyword: Hearing
Link ID: 24021 - Posted: 09.01.2017

Jud Esty-Kendall Josh Hanagarne, 39, and his son Max, 9, recently sat down at StoryCorps to talk about Tourette's syndrome. Josh has dealt with Tourette's since he was Max's age and while Max hasn't been officially diagnosed, he has started to show symptoms, too. Courtesy of StoryCorps Josh Hanagarne is a dad, a librarian and an author, who also has an extreme form of Tourette's syndrome. But he doesn't let it and his tics — his involuntary movements and sounds — stop him from living his life. He says he actually chose to work in a library because it was the quietest place he knew of. Josh first started showing symptoms of Tourette's syndrome when he was in elementary school, about the same age that his son Max is now. Not everyone with Tourette's syndrome has the same tics. Max, 9, describes his dad's as "you hitting yourself and making a lot of noise." "You've seen me hit myself hard enough to almost knock myself out," Josh, 39, says. "I also do all of the blinking and the face things and the little ahem noises." Josh's form of Tourette's is so extreme that his tics have been severe enough that they've put him in the hospital before. "To me, it feels like when you have that urge to sneeze so bad that you just feel like you'll just go insane if you don't let the sneeze out," Josh says. But he says that's not the most difficult part of living with Tourette's. "The hardest thing I do every day is decide to go outside or not, because I know when I walk into a group of strangers, I will yell or I will do something weird and they will all look at me," Josh says. © 2017 npr

Keyword: Tourettes
Link ID: 24020 - Posted: 09.01.2017

Ewen Callaway Japanese researchers report promising results from an experimental therapy for Parkinson’s disease that involves implanting neurons made from ‘reprogrammed’ stem cells into the brain. A trial conducted in monkeys with a version of the disease showed that the treatment improved their symptoms and seemed to be safe, according to a report published on 30 August in Nature1. The study’s key finding — that the implanted cells survived in the brain for at least two years without causing any dangerous effects in the body — provides a major boost to researchers’ hopes of testing stem-cell treatments for Parkinson’s in humans, say scientists. Jun Takahashi, a stem-cell scientist at Kyoto University in Japan who led the study, says that his team plans to begin transplanting neurons made from induced pluripotent stem (iPS) cells into people with Parkinson’s in clinical trials soon. The research is also likely to inform several other groups worldwide that are testing different approaches to treating Parkinson’s using stem cells, with trials also slated to begin soon. Parkinson’s is a neurodegenerative condition caused by the death of cells called dopaminergic neurons, which make a neurotransmitter called dopamine in certain areas of the brain. Because dopamine-producing brain cells are involved in movement, people with the condition experience characteristic tremors and stiff muscles. Current treatments address symptoms of the disease but not the underlying cause. © 2017 Macmillan Publishers Limited,

Keyword: Parkinsons; Stem Cells
Link ID: 24019 - Posted: 08.31.2017

By Ryan Cross Weight loss seems to come easiest to those who want it least. Every year, hundreds of thousands suffer from the loss of appetite that comes with tumor-induced anorexia, which can accompany many late-stage cancers. Now, researchers from three major pharmaceutical companies have independently published papers showing that the culprit behind this condition—a protein called growth differentiation factor-15 (GDF15)—helps mice, rats, and monkeys lose weight without any apparent side effects. “The idea of having another medication to add to our armamentarium is exciting news,” says Katherine Saunders, an obesity medicine physician at Weill Cornell Medicine in New York City who was not involved with the work. There are currently five U.S. Food and Drug Administration–approved obesity medications for long-term weight management, which can help patients lose 5% to 8% of their body weight on average. “That’s very limited,” Saunders says, adding that many drugs used to treat obesity don’t have the same level of specificity as GDF15. GDF15’s potential as a weight-loss agent was first discovered by Samuel Breit, an immunologist and physician at St. Vincent's Hospital in Sydney, Australia. He saw levels of the protein rise 10 to 100 times higher than normal during tumor-induced anorexia in mice with prostate tumors and in humans with advanced prostate cancer. Breit also showed that GDF15 likely exerts its effects through the brain—though he says that until now the protein’s target has befuddled scientists. © 2017 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 24018 - Posted: 08.31.2017

By Colin Hendrie and Alisdair Pickles The current global crisis of depressive illness has a simple root cause: a failure of treatment. This is the result of a broken scientific process that has for nearly 70 years fallen short in delivering the drug therapies it was set up to provide. Given existing antidepressants don’t work for many people, the excitement surrounding the development of a new class of treatments from recreational drugs such as magic mushrooms is understandable. But there are strong reasons to doubt they will have the kind of impact hoped for. Instead, we are more likely to be seeing the latest episode in a long-running saga of repeated disappointment. This saga began when antidepressant use became widespread in the 1950s and 1960s. It was hoped they would have the same transformative effect on mental illness that antibiotics had on non-viral infectious diseases. As it turned out, antidepressants were only of value to some people with depression. Studies involving thousands of people with the condition reveal that the proportion seeing a clinically significant response to antidepressants is often very similar to that seen with a placebo, which is about 40 per cent. In double-blind, placebo-controlled studies, antidepressants don’t fare well. This helps to explain why, by the end of the 20th century, Big Pharma was floundering over the development of new drugs for depression. In 2010, many companies stopped such work. © Copyright New Scientist Ltd.

Keyword: Depression; Drug Abuse
Link ID: 24017 - Posted: 08.31.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

Keyword: Parkinsons; Brain imaging
Link ID: 24016 - Posted: 08.31.2017

BY Patrick Skerrett, An international study is casting doubt on the wisdom of eating lots of carbohydrates. Photo by Flickr user Dani Armengol Garreta Fat, once a dirty word when it came to diet, has been edging back toward respectability. New results from a huge international study help continue to reshape its image while at the same time casting doubt on the wisdom of eating lots of carbohydrates and questioning the “more is better” recommendations for eating fruits and vegetables. The latest evidence comes from data released Tuesday by the international Prospective Urban Rural Epidemiology (PURE) study. Its research team recorded the eating habits of 135,000 adults in 18 countries — including high-income, medium-income, and low-income nations — and followed the participants’ health for more than seven years on average. Among the PURE participants, those with the highest intake of dietary fat (35 percent of daily calories) were 23 percent less likely to have died during the study period than those with the lowest fat intake (10 percent of calories). The rates of various cardiovascular diseases were essentially the same across fat intake, while strokes were less common among those with a high fat intake. Upending conventional wisdom, the findings for carbohydrate intake went in the opposite direction. PURE participants with the highest carbohydrate intake (77 percent of daily calories) were 28 percent more likely to have died than those with the lowest carbohydrate intake (46 percent of calories). The results were presented at the European Society of Cardiology meeting in Barcelona, and published in the Lancet. © 1996 - 2017 NewsHour Productions LLC.

Keyword: Obesity
Link ID: 24015 - Posted: 08.31.2017

By The Scientist Staff Researchers demonstrated that the mouse subiculum, a brain region associated with the hippocampus, is important for recalling certain types of memories, but it doesn’t appear to play a role in forming them. When they optogenetically turned off neurons within the subiculum, mice’s abilities to retrieve a memory they had previously formed was disrupted. Some scientists think that brain circuits responsible for forming memories are the same as those necessary for retrieving them, write the authors in their report. These data, however, offer evidence to the contrary. See D.S. Roy et al., “Distinct neural circuits for the formation and retrieval of episodic memories,” Cell, doi:10.1016/j.cell.2017.07.013, 2017. © 1986-2017 The Scientist

Keyword: Learning & Memory; Brain imaging
Link ID: 24014 - Posted: 08.31.2017

By Meredith Wadman Luca Rossi tried to hang himself in a bedroom in Perugia, Italy, in 2012. Suspended by his belt from a wardrobe, he had begun to choke when his fiancée unexpectedly walked in. He struggled to safety, defeated even in this intended last act. The 35-year-old physician had everything to live for: a medical career, plans for a family, and supportive parents. But Rossi* was addicted to crack cocaine. He had begun his habit not long after medical school, confidently assuming that he could control the drug. Now, it owned him. Once ebullient and passionate, he no longer smiled or cried. He knew he might be endangering his patients, but even that didn’t matter. He was indifferent to all except obtaining his next fix. “It pushes you to suicide because it fills you with your own emptiness,” he says. In the first months after his near suicide, Rossi didn’t drop his $3500-a-month habit. Early in 2013, he learned that his fiancée was pregnant. Frightened by impending fatherhood, he smoked even more. He didn’t—couldn’t—stop. Then, in April 2013, Rossi’s father, a chemist, happened upon a local newspaper article describing work just published in Nature. Neuroscientists led by Antonello Bonci and Billy Chen at the National Institute on Drug Abuse (NIDA) in Baltimore, Maryland, had studied rats trained to seek cocaine compulsively—animals so powerfully addicted that they tolerated repeated electric shocks to their feet to get their fixes. The rats had also been genetically engineered so that their neurons could be controlled with light. When the researchers stimulated the animals’ brains in an area that regulates impulse control, the rats essentially kicked their habit. “They would almost instantaneously stop searching for cocaine,” Bonci says. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging; Drug Abuse
Link ID: 24013 - Posted: 08.30.2017